ArticlePloS one2011
NF-κB inducing kinase, NIK mediates cigarette smoke/TNFα-induced histone acetylation and inflammation through differential activation of IKKs.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 52 citations in OpenAlex.
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- Lactylation at the crossroads of immune metabolism and epigenetic regulation: revealing its role in rheumatic immune diseases.Journal of translational medicine · 2025Review
- A new type of Caspase-1 upon recognizing bacteria inhibits GSDME-dependent histone modification and NF-κB signaling.Communications biology · 2025Article
- Effects of Combustible Cigarettes and Heated Tobacco Products on Systemic Inflammatory Response in Patients with Chronic Inflammatory Diseases.Diseases (Basel, Switzerland) · 2024Article
- Epigenetic regulation of pulmonary inflammation.Seminars in cell & developmental biology · 2024Review
- Epigenetic targets to enhance antitumor immune response through the induction of tertiary lymphoid structures.Frontiers in immunology · 2024Review
- Review
- The role of cigarette smoke-induced epigenetic alterations in inflammation.Epigenetics & chromatin · 2019Review
- Andrographolide inhibits breast cancer through suppressing COX-2 expression and angiogenesis via inactivation of p300 signaling and VEGF pathway.Journal of experimental & clinical cancer research : CR · 2018Article
- IL-17A-associated IKK-α signaling induced TSLP production in epithelial cells of COPD patients.Experimental & molecular medicine · 2018Article
- Memory Training Program Decreases the Circulating Level of Cortisol and Pro-inflammatory Cytokines in Healthy Older Adults.Frontiers in molecular neuroscience · 2017Article
- Gene expression profiling of epigenetic chromatin modification enzymes and histone marks by cigarette smoke: implications for COPD and lung cancer.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- MicroRNA-223 controls the expression of histone deacetylase 2: a novel axis in COPD.Journal of molecular medicine (Berlin, Germany) · 2016Article
- FoxO1 regulates allergic asthmatic inflammation through regulating polarization of the macrophage inflammatory phenotype.Oncotarget · 2016Article
- Circadian molecular clock in lung pathophysiology.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Distinct role of FoxO1 in M-CSF- and GM-CSF-differentiated macrophages contributes LPS-mediated IL-10: implication in hyperglycemia.Journal of leukocyte biology · 2015Article
- Cigarette smoke induces distinct histone modifications in lung cells: implications for the pathogenesis of COPD and lung cancer.Journal of proteome research · 2014Article
- Protective effects of bifidobacterial adhesin on intestinal mucosa of stressed male rats via modulation of inflammation.International journal of clinical and experimental pathology · 2014Article
- TWEAK/Fn14 and Non-Canonical NF-kappaB Signaling in Kidney Disease.Frontiers in immunology · 2013Review
- Neu-164 and Neu-107, two novel antioxidant and anti-myeloperoxidase compounds, inhibit acute cigarette smoke-induced lung inflammation.American journal of physiology. Lung cellular and molecular physiology · 2013Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundNuclear factor (NF)-κB inducing kinase (NIK) is a central player in the non-canonical NF κB pathway, which phosphorylates IκB kinase α (IKKα) resulting in enhancement of target gene expression. We have recently shown that IKKα responds to a variety of stimuli including oxidants and cigarette smoke (CS) regulating the histone modification in addition to its role in NF-κB activation. However, the primary signaling mechanism linking CS-mediated oxidative stress and TNFα with histone acetylation and pro-inflammatory gene transcription is not well understood. We hypothesized that CS and TNFα increase NIK levels causing phosphorylation of IKKα, which leads to histone acetylation. METHODOLOGY: To test this hypothesis, we investigated whether NIK mediates effects of CS and TNFα on histone acetylation in human lung epithelial cells in vitro and in lungs of mouse exposed to CS in vivo. CS increased the phosphorylation levels of IKKα/NIK in lung epithelial cells and mouse lungs. NIK is accumulated in the nuclear compartment, and is recruited to the promoters of pro-inflammatory genes, to induce posttranslational acetylation of histones in response to CS and TNFα. Cells in which NIK is knocked down using siRNA showed partial attenuation of CSE- and TNFα-induced acetylation of histone H3 on pro-inflammatory gene promoters. Additional study to determine the role of IKKβ/NF-κB pathway in CS-induced histone acetylation suggests that the canonical pathway does not play a role in histone acetylation particularly in response to CS in mouse lungs.
conclusionsOverall, our findings provide a novel role for NIK in CS- and TNFα-induced histone acetylation, especially on histone H3K9.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.